pituitrin and Nausea

Topics: Electrophysiology; Humans; Nausea; Stomach Diseases; Vasopressins

The functional characteristics of osmoregulated vasopressin secretion can be defined in terms of an osmotic threshold for its release and a sensitivity of the osmoreceptor and vasopressin-secreting unit. Osmotically stimulated thirst has features similar to osmoregulated vasopressin. There are wide individual variations in the functional characteristics of both thirst and vasopressin release in healthy humans, probably genetic in origin. The influence of aging appears to enhance the sensitivity of vasopressin secretion but blunt thirst appreciation. Yet in many physiological situations changes in osmoregulated vasopressin release and thirst occur in parallel. The fall in plasma osmolality associated with human pregnancy is accounted for entirely by a lowering of the osmotic thresholds for thirst and vasopressin release. Similar but less marked alterations accompany the ovulatory luteal phase of the menstrual cycle. A major nonosmotic stimulus to vasopressin secretion is hypotension and/or hypovolemia, mediated by high- (carotid sinus) and low- (left atrial) pressure receptors. Circulating catecholamines influence the release of vasopressin by alpha- and beta-adrenergic pathways. Drinking by hypertonic humans provides immediate reduction in thirst and vasopressin secretion probably mediated by pathways from the oropharynx. The modest but variable rise in plasma vasopressin in response to hypoglycemia appears to be due to cellular neuroglycopenia and is independent of parasympathetic pathways. Although osmotic and hemodynamic stimuli to vasopressin release do not act independently of each other, the precise subtle interactions between them and other nonosmotic stimuli remain to be clarified.

Topics: Drinking; Humans; Hypoglycemia; Nausea; Pressoreceptors; Thirst; Vasopressins; Vomiting; Water-Electrolyte Balance

Topics: Animals; Blood; Blood Pressure; Blood Volume; Diabetes Insipidus; Diuresis; Female; Humans; Hyperaldosteronism; Hypernatremia; Hyponatremia; Hypothalamus; Lung Neoplasms; Nausea; Osmolar Concentration; Pituitary Gland, Posterior; Pregnancy; Pressoreceptors; Sodium; Thirst; Urine; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Stress hormones might be involved in motion sickness. The influence of loperamide on kinetosis-induced nausea and stress hormone release was investigated in a placebo-controlled, cross-over study.. Standardized rotation around the vertical axis combined with head movements was used to induce nausea 3 h after 16 mg loperamide or placebo (n = 8). Plasma antidiuretic hormone (ADH), adrenocorticotropic hormone (ACTH) and nausea ratings were investigated.. After loperamide nausea was significantly lower (P < 0.02). ACTH (P < 0.05) and ADH levels (P < 0.02) increased significantly in both settings, but were lower after loperamide.. The susceptibility to develop kinetosis-induced nausea and stress hormone release is decreased by loperamide, although the site of action remains speculative.

Topics: Adrenocorticotropic Hormone; Adult; Cross-Over Studies; Female; Humans; Loperamide; Male; Motion Sickness; Nausea; Receptors, Opioid, mu; Rotation; Single-Blind Method; Vasopressins

The mechanism of the antiemetic actions of corticosteroids is not known. The purpose of this study was to evaluate if betamethasone can prevent nausea, vomiting or increase of vasopressin induced by apomorphine. Metoclopramide, a dopamine antagonist, was used as a control substance.. Ten healthy volunteers were studied on three occasions. In a randomized order they were allocated to receive pretreatment with betamethasone 8 mg iv, metoclopramide 10 mg iv, and normal saline 2 mL as placebo on the three different occasions, 15 min before the administration of apomorphine 30 microg x kg(-1) s.c.. After administration of apomorphine, episodes of vomiting were recorded, and the intensity of nausea was estimated by the subject on a visual analogue scale (VAS 0-10 cm). Blood samples for analysis of plasma concentrations of vasopressin were analyzed.. One volunteer decided to withdraw, as he experienced akathisia after receiving metoclopramide. During the first two hours after apomorphine, eight of nine volunteers vomited both after betamethasone and placebo. One volunteer did not vomit after betamethasone and placebo but he experienced nausea. None of the volunteers vomited after metoclopramide (P < 0.01 vs betamethasone and placebo). The maximum VAS for nausea was significantly higher after betamethasone and placebo compared to metoclopramide (P < 0.01). The vasopressin levels increased after betamethasone and placebo, but there was no increase in any volunteer after pretreatment with metoclopramide.. This study demonstrates that betamethasone does not prevent nausea, vomiting and increase of vasopressin induced by apomorphine, whereas metoclopramide prevents apomorphine-induced emesis. Our work suggests that betamethasone does not have dopamine-antagonistic effects.

Topics: Adult; Apomorphine; Betamethasone; Dopamine Agonists; Dopamine Antagonists; Female; Glucocorticoids; Humans; Male; Metoclopramide; Nausea; Pain Measurement; Reference Values; Severity of Illness Index; Time Factors; Treatment Outcome; Vasopressins; Vomiting

Ginger has long been used as an alternative medication to prevent motion sickness. The mechanism of its action, however, is unknown. We hypothesize that ginger ameliorates the nausea associated with motion sickness by preventing the development of gastric dysrhythmias and the elevation of plasma vasopressin. Thirteen volunteers with a history of motion sickness underwent circular vection, during which nausea (scored 0-3, i.e., none to severe), electrogastrographic recordings, and plasma vasopressin levels were assessed with or without ginger pretreatment in a crossover-design, double-blind, randomized placebo-controlled study. Circular vection induced a maximal nausea score of 2.5 +/- 0.2 and increased tachygastric activity and plasma vasopressin. Pretreatment with ginger (1,000 and 2,000 mg) reduced the nausea, tachygastria, and plasma vasopressin. Ginger also prolonged the latency before nausea onset and shortened the recovery time after vection cessation. Intravenous vasopressin infusion at 0.1 and 0.2 U/min induced nausea and increased bradygastric activity; ginger pretreatment (2,000 mg) affected neither. Ginger effectively reduces nausea, tachygastric activity, and vasopressin release induced by circular vection. In this manner, ginger may act as a novel agent in the prevention and treatment of motion sickness.

Topics: Adolescent; Adult; Double-Blind Method; Electrophysiology; Female; Humans; Infusions, Intravenous; Male; Motion; Motion Sickness; Nausea; Phytotherapy; Rotation; Stomach; Vasopressins; Zingiber officinale

The aim of this study was to compare micropuncture laparoscopic cholecystectomy (MPLC), with three 3.3-mm cannulas and one 10-mm cannula with conventional laparoscopic cholecystectomy (CLC).. Patients were randomized to undergo either CLC or MPLC. The duration of each operative stage and the procedure were recorded. Interleukin-6 (IL-6), adrenocorticotropic hormone (ACTH), and vasopressin were sampled for 24 h. Visual analogue pain scores (VAPS) and analgesic consumption were recorded for 1 week. Pulmonary function and quality of life (EQ-5D) were monitored for 4 weeks. Statistical analysis was performed using the Mann-Whitney test or Fisher's exact test. Results are expressed as median (interquartile range).. Forty-four patients entered the study, but four were excluded due to unsuspected choledocholithiasis (n = 3) or the need to reschedule surgery (n = 1). The groups were comparable in terms of age, duration of symptoms, and indications for surgery. Total operative time was similar (CLC, 63 [52-81] min vs MPLC 74 [58-95] min; p = 0.126). However, time to place the cannulas after skin incision (CLC, 5:42 [3:45-6:37] min vs MPLC, 7:38 [5:57-10:15] min; p = 0.015) and to clip the cystic duct after cholangiography (CLC, 1:05 [0:40-1:35] min vs MPLC, 3:45 [2:26-7:49] min; p <0.001) were significantly longer for MPLC. Six CLC patients and one MPLC patient required postoperative parenteral opiates (p = 0.04). Oral analgesic consumption was similar in both groups (p = 0.217). Median VAPS were lower at all time points for MPLC, but this finding was not significant (p = 0.431). There were no significant differences in postoperative stay, IL-6, ACTH or vasopressin responses, pulmonary function, or EQ-5D scores.. The thinner instruments did not significantly increase the total duration of the procedure. MPLC reduced the use of parenteral analgesia postoperatively, which may prove beneficial for day case patients, but it did not have a significant impact on laboratory variables, lung function or quality of life.

Topics: Adrenocorticotropic Hormone; Adult; Analgesia; Cholecystectomy; Cholecystectomy, Laparoscopic; Gallbladder; Humans; Interleukin-6; Middle Aged; Nausea; Pain Measurement; Postoperative Complications; Punctures; Quality of Life; Respiratory Function Tests; Stress, Physiological; Vasopressins; Vomiting

In vitro studies in hypothalamic-pituitary explants in the rat have suggested cholinergic mediation of arginine vasopressin (AVP) osmoregulation. In this study we attempted to demonstrate, in humans, cholinergic mediation of AVP osmoregulation. Specifically, we tested the hypothesis that the plasma AVP response to an osmolar stimulus would be attenuated by pharmacologic blockade of central nervous system muscarinic or nicotinic receptors in humans. We also evaluated the effects of cholinergic blockade on the norepinephrine (NE) response to an osmolar stimulus. Young normal males underwent hypertonic saline infusion following administration of the centrally active muscarinic antagonist scopolamine or the centrally active nicotinic antagonist mecamylamine. Neither mecamylamine nor scopolamine affected the AVP response to hypertonic saline infusion. Mecamylamine reduced NE concentrations in a dose-dependent manner, but did not affect the slope of the NE increase during hypertonic saline infusion. In a second experiment, we evaluated the effects of scopolamine and mecamylamine on the AVP and NE responses to physostigmine, a cholinesterase inhibitor which stimulates AVP release into plasma through a non-osmolar central nervous system cholinergic mechanism. Scopolamine eliminated the AVP response to physostigmine. Mecamylamine reduced NE concentrations both before and after scopolamine administration but did not affect the slope of the AVP response. These results fail to support cholinergic regulation of the AVP response to osmolar stimulation in humans.

Topics: Adult; Blood Pressure; Cholinesterase Inhibitors; Humans; Male; Nausea; Norepinephrine; Parasympathetic Nervous System; Parasympatholytics; Physostigmine; Receptors, Muscarinic; Receptors, Nicotinic; Saline Solution, Hypertonic; Scopolamine; Vasopressins

Nausea is a common prodromal symptom of neurally mediated syncope, but the biological factors linking nausea with syncope have not been studied. We aimed to characterize nausea during tilt-induced syncope by exploring related changes in gastric myoelectrical activity and plasma epinephrine, norepinephrine, and vasopressin concentrations across study phases of recumbency, tilt, syncope, and recovery.. Electrogastrographic and plasma hormone changes were compared between patients with tilt-induced syncope and nausea (n = 18) and control subjects (n = 6) without symptoms or hemodynamic changes during tilt-table testing.. Over a 4-minute period preceding syncope, sequential electrogastrography epochs demonstrated an increase over time in bradygastria (P = .003) and tachygastria (P = .014) power ratios, while the dominant frequency (P < .001) and the percent normogastria (P = .004) decreased. Syncope led to significant differences between cases and controls in electrogastrographic power ratios in each frequency range: bradygastria (P = .001), tachygastria (P = .005), and normogastria (P = .03). Nausea always followed electrogastrographic changes, and nausea resolution always preceded electrogastrographic normalization. Plasma vasopressin (676.5 ± 122.8 vs 91.2 ± 15.3 pg/mL, P = .012) and epinephrine (434 ± 91.3 vs 48.7 ± 2.5 pg/mL, P = .03), but not norepinephrine (P > .05), also differed with syncope between cases and controls.. The nausea related to tilt-induced syncope is temporally associated with changes in gastric myoelectrical activity and increases in plasma vasopressin and epinephrine. The biological mechanisms that induce syncope are physiologically distinct from other experimental models of nausea such as illusory self-motion, yet nausea with syncope appears to have similarly associated electrogastrographic and hormone changes. Thus, tilt-induced syncope could serve as an informative experimental model for nausea research.

Topics: Adolescent; Electromyography; Epinephrine; Female; Humans; Nausea; Norepinephrine; Stomach; Syncope; Tilt-Table Test; Vasopressins

Chronic nausea in pediatrics is a debilitating condition with unclear etiology. We aimed to define hemodynamic and neurohumoral characteristics of chronic nausea associated with orthostatic intolerance in order to improve identification and elucidate mechanism.. Children (10-18 years) meeting Rome III criteria for functional dyspepsia with nausea and symptoms of orthostatic intolerance (OI) completed a Nausea Profile Questionnaire followed by prolonged (45 minutes rather than the traditional 10 minutes) head-upright tilt (HUT) (70° tilt up) test. Circulating catecholamines, vasopressin, aldosterone, renin, and angiotensins were measured supine and after 15 minutes into HUT. Beat-to-beat heart rate and blood pressure were continuously recorded to calculate their variability and baroreflex sensitivity.. Within 10 and 45 minutes of HUT, 46% and 85% of subjects, respectively, had an abnormal tilt test (orthostatic hypotension, postural orthostatic tachycardia, or syncope). At 15 and 45 minutes of HUT, nausea was elicited in 42% and 65% of subjects respectively. Higher Nausea Profile Questionnaire scores correlated with positive HUT testing at 10 minutes (P = 0.004) and baroreflex sensitivity at 15 minutes (P ≤ 0.01). Plasma vasopressin rose 33-fold in subjects with HUT-induced nausea compared to twofold in those who did not experience HUT-induced nausea (P < 0.01).. In children with chronic nausea and OI, longer duration HUT elicited higher frequency of abnormal tilt testing and orthostatic-induced nausea. The Nausea Profile Questionnaire predicted the orthostatic response to tilt testing. Exaggerated vasopressin release differentiated patients with HUT-induced nausea (vs those without nausea), suggesting a possible mechanism for chronic nausea in childhood.

Topics: Adolescent; Child; Female; Humans; Male; Nausea; Orthostatic Intolerance; Surveys and Questionnaires; Tilt-Table Test; Vasopressins

An integrated understanding of the physiological mechanisms involved in the genesis of nausea remains lacking. We aimed to describe the psychophysiological changes accompanying visually induced motion sickness, using a motion video, hypothesizing that differences would be evident between subjects who developed nausea in comparison to those who did not. A motion, or a control, stimulus was presented to 98 healthy subjects in a randomized crossover design. Validated questionnaires and a visual analogue scale (VAS) were used for the assessment of anxiety and nausea. Autonomic and electrogastrographic activity were measured at baseline and continuously thereafter. Plasma vasopressin and ghrelin were measured in response to the motion video. Subjects were stratified into quartiles based on VAS nausea scores, with the upper and lower quartiles considered to be nausea sensitive and resistant, respectively. Twenty-eight subjects were exposed to the motion video during functional neuroimaging. During the motion video, nausea-sensitive subjects had lower normogastria/tachygastria ratio and cardiac vagal tone but higher cardiac sympathetic index in comparison to the control video. Furthermore, nausea-sensitive subjects had decreased plasma ghrelin and demonstrated increased activity of the left anterior cingulate cortex. Nausea VAS scores correlated positively with plasma vasopressin and left inferior frontal and middle occipital gyri activity and correlated negatively with plasma ghrelin and brain activity in the right cerebellar tonsil, declive, culmen, lingual gyrus and cuneus. This study demonstrates that the subjective sensation of nausea is associated with objective changes in autonomic, endocrine and brain networks, and thus identifies potential objective biomarkers and targets for therapeutic interventions.

Topics: Adult; Autonomic Nervous System; Case-Control Studies; Cerebral Cortex; Endocrine System; Female; Ghrelin; Humans; Male; Middle Aged; Motion Sickness; Nausea; Vasopressins

Diabetes insipidus (DI) is a rare clinical condition, which is usually caused by neurohypophyseal or pituitary stalk infiltration in cancer patients.. we present a 62-year old metastatic breast cancer woman with DI. She admitted to the hospital because of nausea, vomiting, polyuria and polydipsia, while she was on no cytotoxic medication. She had no electrolyte imbalance except mild hypernatremia. The CT scan of the brain yielded a suspicious area in pituitary gland. A pituitary stalk metastasis was found on magnetic resonance imaging (MRI) of pituitary. Water deprivation test was compatible with DI. A clinical response to nasal vasopressin was achieved.. Cancer patients who have symptoms such as nausea, vomiting, polyuria and polydipsia while they are not on chemotherapy should be evaluated for not only metabolic complications like hypercalcemia but also posterior pituitary or stalk metastasis MRI could be the choice of imaging for pituitary metastasis.

Topics: Administration, Intranasal; Breast Neoplasms; Diabetes Insipidus; Female; Humans; Magnetic Resonance Imaging; Nausea; Pituitary Neoplasms; Polyuria; Thirst; Vasopressins; Vomiting

It has been shown that stress changes stimulated pro-inflammatory cytokine production and the sensitivity of stimulated cytokine production to glucocorticoid suppression. While glucocorticoid secretion habituates in response repeated stimulation, it is not known whether stimulation and suppression of cytokine production are also subject to adaptation. Eight healthy young subjects were exposed to repeated nauseogenic body rotation on four consecutive days. On each day subjects were rotated around the vertical axis up to five times for a period of 1 min or until subjects chose to stop due to nausea. Blood and saliva samples were obtained before and after rotation for assessment of cortisol, ACTH, plasma vasopressin (ADH), in vitro TNF-alpha and IL-6 production and glucocorticoid sensitivity of TNF-alpha and IL-6 production. Rotation induced increases of ACTH, cortisol, and ADH in the first session. All endocrine responses habituated over time, except for the free cortisol response in men. Pro-inflammatory cytokine production showed a sex-specific response pattern with increases in men and decreases in women in the first session vs. increases in men and women in the last session. Response patterns of GC sensitivity also changed over time: in the first session, sensitivity increased only in men, but in the last session, GC sensitivity decreased in all subjects. In conclusion, in response to repeated nausea induction, habituation occurs only in the endocrine system and predominantly in women. In the immune system, response patterns change in the favor of inflammatory conditions, with increases in stimulated IL-6 and TNF-alpha and decreases in the effectiveness of glucocorticoid suppression of these cytokines. These presumably unfavorable changes in the inflammatory system are more pronounced men.

Topics: Adaptation, Physiological; Adrenocorticotropic Hormone; Adult; Cytokines; Female; Humans; Hydrocortisone; Interleukin-6; Male; Motion Sickness; Nausea; Reference Values; Rotation; Saliva; Sex Factors; Tumor Necrosis Factor-alpha; Vasopressins

The aims of this study were to investigate the effects and mechanisms of a novel method of gastric electrical stimulation on the prevention of vasopressin-induced emetic response and gastric dysrhythmias.. Fifteen dogs (10 normal, 5 vagotomized) chronically implanted with gastric serosal electrodes were used in a 3-session study (vasopressin, vasopressin plus 2-channel stimulation [DCS], and vasopressin plus dual-pulse stimulation [DPS]).. Vasopressin induced gastric dysrhythmias and motion sickness-like symptoms (P < .05) and these effects were blocked partially with vagotomy. Both methods of DCS and DPS were capable of preventing vasopressin-induced gastric dysrhythmias (P < .05) and motion sickness-like symptoms (P < .05). The antiemetic effects of the proposed methods of DCS and DPS were abolished by vagotomy but their antidysrhythmic effects were not blocked by vagotomy.. DCS and DPS are able to reduce vasopressin-induced gastric dysrhythmia and symptoms of nausea and vomiting. The vagal pathway is involved in the antiemetic effect but not the antidysrhythmic effect of the proposed methods of stimulation.

Topics: Animals; Dogs; Electric Stimulation Therapy; Female; Nausea; Stomach; Stomach Diseases; Vagotomy; Vasopressins; Vomiting

The aim of this study was to investigate the acute effects of 3 different methods of electrical stimulation in the prevention of vasopressin-induced emetic response and gastric dysrhythmias.. Seven female hound dogs chronically implanted with 4 pairs of electrodes on gastric serosa were used in a 5-session study. Saline and vasopressin were infused in sessions 1 and 2, respectively. In the other 3 sessions with vasopressin infusion, 3 different methods of electrical stimulation (short-pulse stimulation, long-pulse stimulation, and electroacupuncture) were applied. Gastric slow waves and vomiting and behaviors suggestive of nausea were recorded in each session. In a separate study, additional experiments were performed in 5 vagotomized dogs to investigate vagally mediated mechanisms.. Vasopressin induced gastric dysrhythmias, uncoupling of slow waves, and vomiting and behaviors suggestive of nausea (P < 0.02, analysis of variance). Long-pulse stimulation, but not short-pulse stimulation or electroacupuncture, was capable of preventing vasopressin-induced gastric dysrhythmias and gastric slow wave uncoupling. Short-pulse stimulation and electroacupuncture, but not long-pulse stimulation, prevented vomiting and significantly reduced the symptom scores, which was not noted in the dogs with truncal vagotomy.. Long-pulse stimulation normalizes vasopressin-induced slow wave abnormalities with no improvement in vomiting and behaviors suggestive of nausea. Short-pulse stimulation and electroacupuncture prevent vomiting and behaviors suggestive of nausea induced by vasopressin but have no effects on slow waves, and their effects are vagally mediated.

Topics: Animals; Behavior, Animal; Dogs; Electric Stimulation Therapy; Electroacupuncture; Electrophysiology; Female; Nausea; Periodicity; Stomach; Stomach Diseases; Vagotomy; Vasopressins; Vomiting

The possible role of vasopressin in nausea and gastric dysrhythmias in motion sickness was tested by electrogastrography in 14 subjects during circular vection (60 degrees/s) and vasopressin infusion. Tachygastria was expressed as the signal percent >4.5 cycles/min. Vection evoked nausea scores of 2.6 +/- 0.2 (0 = none to 3 = severe) in 10 subjects with increases in tachygastric activity (15 +/- 2 to 45 +/- 3%) and plasma vasopressin (4.5 +/- 1.5 to 8.4 +/- 2.5 pg/ml) that were blocked by atropine but not indomethacin. Four asymptomatic subjects had no tachygastria or vasopressin release. Vasopressin at 0.2 U/min (plasma level = 322.1 +/- 10.3 pg/ml) evoked nausea (2.6 +/- 0.4) and increases in tachyarrhythmic activity (41 +/- 5%) that were blunted by atropine but not indomethacin. There were no differences in nausea or dysrhythmias with vasopressin infusion in subjects who noted nausea during vection versus those who did not. To conclude, vection evokes nausea, dysrhythmias, and vasopressin release in motion sickness-susceptible humans via cholinergic prostaglandin-independent pathways. Supraphysiological vasopressin infusions evoke nausea and dysrhythmias by similar pathways to equal degrees in motion sickness-susceptible and -resistant subjects. Thus central but not peripheral actions of vasopressin may contribute to nausea and slow wave disruption with vection. Blunting of both the release and action of vasopressin by atropine may explain its beneficial action in motion sickness.

Topics: Adult; Atropine; Cyclooxygenase Inhibitors; Female; Humans; Indomethacin; Male; Motion Sickness; Nausea; Parasympatholytics; Periodicity; Rotation; Stomach; Vasopressins

The standard human vection model utilized for nausea has been an optokinetic drum. This model may be difficult to extrapolate to the usual clinical setting. Our goals were to develop an experimental model which could induce low grade nausea in humans and to determine the relationship between mild nausea and changes in the electrogastrogram and plasma vasopressin concentrations.. Twenty-one volunteers (11 males, mean age: 37 years) participated. At baseline and throughout the study the electrogastrogram was monitored, blood was drawn for vasopressin assay and symptoms of nausea, dizziness and headache were rated on a 0-10-point scale. Subjects were semireclined in a darkened room while viewing moving bars of light rotating at a rate of 85 degrees s-1. Subjects were asked to rate their proneness to motion sickness and their current level of anxiety at baseline.. Eight subjects developed mild to moderate (mean: 3.6) nausea during vection. Symptoms of nausea were correlated with a reported history of motion sickness (r = 0.49, P < 0.05) but not with anxiety (r = 0.14, P = 0.54). Degrees of nausea correlated with degrees of dizziness (r = 0.47, P < 0.05) but not with headache (r = 0.29, P = 0.14). Subjects who developed mild nausea were not significantly more likely to exhibit altered electrogastrogram or vasopressin than subjects who did not report nausea. Vasopressin levels during baseline and experimental conditions were highly correlated (r = 0.66, P < 0.005 and r = 0.55 P < 0.005, respectively) with reported baseline anxiety.. (1) This new model in humans induced mild nausea that was unrelated to electrogastrogram and vasopressin abnormalities, (2) high correlation between anxiety and vasopressin suggests that vasopressin may not be directly related to nausea, and (3) these data indicate that onset of nausea mediated centrally can occur without associated electrogastrogram changes.

Topics: Adult; Aged; Anxiety; Dizziness; Electromyography; Female; Headache; Humans; Illusions; Male; Middle Aged; Models, Biological; Motion Sickness; Muscle, Smooth; Myoelectric Complex, Migrating; Nausea; Nystagmus, Optokinetic; Reference Values; Regression Analysis; Stomach; Vasopressins

Topics: Diuresis; Humans; Nausea; Vasopressins

Topics: Humans; Nausea; Stomach; Vasopressins

Vasopressin is a vasoactive hormone secreted from the posterior pituitary. At low concentration its role is in regulating renal water excretion, but at higher concentrations it has a number of extrarenal actions, including effects on blood flow. To investigate the role of vasopressin in spontaneous migraine, paired samples were collected from 14 subjects (a) during an acute attack of spontaneous migraine, and (b) when symptom-free for at least seven days. During an attack, vasopressin was consistently raised (median (range) 3.5 (1.2-9.6) pg/ml v 0.5 (0.5-1.1) pg/ml, p less than 0.001). The highest vasopressin concentration occurred in the only patient who vomited. The results suggest vasopressin rises during an attack of spontaneous migraine, and this may, in part, be related to emesis. In the majority, vasopressin levels only rose sufficiently to have some renal antidiuretic effect, although in some these levels could have been sufficient to cause alteration in peripheral blood flow. Release of vasopressin may be responsible for the facial pallor and antidiuresis observed in migraine.

Topics: Adult; Female; Humans; Male; Middle Aged; Migraine Disorders; Nausea; Vasopressins

Vasopressin and oxytocin are nonapeptides secreted from the neurohypophysis; increases in vasopressin are associated with nausea and vomiting in some, but not all, species. Our aim was to determine whether plasma vasopressin and oxytocin levels were altered in healthy volunteers who did or did not develop nausea during vection, an optokinetic stimulus which produces the illusion of self-motion. Vection was produced by rotating a drum with an inner surface of black and white vertical stripes around the seated stationary subject. Gastric myoelectrical activity was recorded continuously throughout the experiment with electrodes positioned on the abdominal surface. Plasma samples were obtained before vection and after drum rotation stopped when nausea and tachygastria were present. Vasopressin and oxytocin were extracted from plasma and quantified by RIA. During vection six subjects reported nausea and developed gastric dysrhythmias; six other subjects had no nausea and remained in normal 3-cpm myoelectrical rhythms. Vasopressin and oxytocin values before vection were similar in each group of subjects. One minute after vection stopped, plasma vasopressin levels were significantly greater (P less than 0.05) in subjects experiencing nausea and tachygastrias (35.4 +/- 26.7 pmol/L) than in those without symptoms (2.7 +/- 0.47 pmol/L). Oxytocin levels were unchanged by either vection or nausea. It is concluded that 1) vasopressin, not oxytocin, neurons in the magnocellular-neurohypophyseal system are activated during vection-induced nausea and gastric dysrhythmias; and 2) illusory self-motion may be used safely to study the neuroendocrine responses to brain-gut interactions and nausea in man.

Topics: Adult; Brain; Digestive System Physiological Phenomena; Female; Humans; Male; Motion Sickness; Nausea; Ovum; Oxytocin; Vasopressins

Based on studies in animals and humans, it has been suggested that nausea activates the hypothalamo-neurohypophyseal system with resultant increases in circulating concentrations of oxytocin or vasopressin. The purpose of these studies was to determine in humans whether nausea is associated with increases in circulating concentrations of neurohypophyseal hormones or various enteropancreatic peptides (vasoactive intestinal polypeptide, substance P, or pancreatic polypeptide). Nausea, induced by intravenous infusion of apomorphine, was associated with fivefold to 75-fold increases in plasma vasopressin concentrations in 7 subjects (mean increase, 41-fold), with no change in plasma oxytocin levels. Furthermore, nausea was associated with sevenfold to 16-fold increases in plasma pancreatic polypeptide concentrations (mean increase, ninefold), with no change in plasma levels of vasoactive intestinal polypeptide or substance P. In 1 subject refractory to nausea, there was no increase in plasma vasopressin or pancreatic polypeptide concentrations with apomorphine. These studies indicate that nausea in humans is associated with vasopressin and pancreatic polypeptide release.

Topics: Adult; Apomorphine; Female; Humans; Infusions, Intravenous; Nausea; Oxytocin; Pancreatic Polypeptide; Substance P; Vasoactive Intestinal Peptide; Vasopressins

Hyponatremia and hypo-osmolality developed in a 70-year-old patient. It was probably mediated by hypersecretion of antidiuretic hormone, which, in turn, was due to prolonged nausea and vomiting. Severe esophagitis was the cause of the nausea. The patient was not given large amounts of fluids intravenously, and it is likely that she continued to drink for nondipsetic reasons. In view of her medical history of neurosyphilis, the possibility of a disturbance in the mechanism of thirst regulation is discussed, but remains unproved.

Topics: Aged; Esophagitis, Peptic; Female; Humans; Hyponatremia; Nausea; Osmolar Concentration; Syndrome; Time Factors; Vasopressins; Vomiting; Water-Electrolyte Imbalance

Eleven randomly hydrated patients with metastatic malignancies received iv bolus chemotherapy. Serial observations of plasma antidiuretic hormone (ADH), serum osmolality, blood pressure, and presence of nausea or emesis were made over the next 3-4 hours. Group 1 (four patients) had no nausea or emesis and no change in ADH, osmolality, or mean blood pressure. Group 2 (seven patients) had nausea and emesis following chemotherapy, with an increase in mean ADH from a baseline level of 5.53 pg/ml to a peak after emesis of 33.83 pg/ml. Group 2 had no significant increase in osmolality or decrease in mean blood pressure before emesis. ADH levels increased 0-40 minutes before emesis and peaked 28-115 minutes (mean, 66) after emesis. Emesis caused by chemotherapy agents is associated with rapid, significant increases in plasma ADH levels, independent of changes in osmolality or blood pressure.

Topics: Antineoplastic Agents; Blood Pressure; Humans; Nausea; Osmolar Concentration; Vasopressins

The mechanisms underlying the frequent association of nausea and vomiting with elevations of plasma vasopressin(PAVP) were studied in man and rat. After oral water loads (N = 16), plasma osmolality fell in all human subjects and was associated with a decline in PAVP in 14 asymptomatic human subjects. In 2 human subjects, nausea occurred and was associated with increases in PAVP, without changes in blood pressure. During ethanol infusion (N = 28), PAVP was suppressed unless nausea supervened. In 4 nauseated human subjects, PAVP escaped from ethanol inhibition and rose to levels 10 times basal, despite the absence of hemodynamic changes. Apomorphine, a potent dopamine agonist and emetic agent, was administered to human volunteers in doses of 7 to 24 microgram/kg. There was no increase in PAVP in 3 human subjects who remained asymptomatic (7 to 16 microgram/kg). Ten human subjects experienced nausea after 16 microgram/kg, which was followed shortly by marked increases in PAVP. Emesis occurred in 5 human subjects given 16 to 24 microgram/kg, and was followed by PAVP levels similar to those seen with nausea alone. In 7 human subjects from the nausea group, the repeat study (16 microgram/kg) after pretreatment with dopamine antagonist (haloperidol, N = 4; fluphenazine, N = 3) resulted in complete blockage of apomorphine-induced AVP release. In rats, which lack an emetic reflex, apomorphine doses of 200 microgram/kg induced only slight increases in PAVP when compared to the response to 16 microgram/kg in man. These studies indicate that stimulation of the emetic reflex results in AVP-release in man. Nausea-mediated AVP release supervenes over concomitant osmolar or pharmacologic (ethanol) inhibition.

Topics: Alcohols; Animals; Apomorphine; Blood Pressure; Diuresis; Female; Humans; Male; Nausea; Rats; Vasopressins; Vomiting; Water

Nalpha-glycyl-glycyl-glycyl-(8-lysine)-vasopressin, a hormone analogue with prolonged pharmacological action due to slow release of active nonapeptide by enzyme action in vivo, has been administered to 5 control subjects and to 14 patients actively bleeding from upper gastrointestinal sites. The control subjects showed a prolonged pressor response to 100mug/kg body weight associated with a rise in cardiac output, with no ECG signs of myocardial toxicity. 13 of the 14 bleeding patients showed not only pressor responses and haemodynamic and clinical improvement when administering doses of 20-100 mug/kg, but clear signs of standstill of upper gastrointestinal bleeding.

Topics: Adolescent; Adult; Aged; Animals; Colic; Defecation; Dogs; Esophageal and Gastric Varices; Female; Gastrointestinal Hemorrhage; Glycine; Heart; Hemodynamics; Humans; Lypressin; Male; Middle Aged; Nausea; Peptic Ulcer Hemorrhage; Sweating; Urination; Vasopressins

Topics: Abdomen; Adult; Blood Pressure; Cardiac Output; Esophageal and Gastric Varices; Female; Headache; Heart Rate; Hemorrhage; Humans; Infusions, Parenteral; Injections, Intravenous; Male; Middle Aged; Muscle Cramp; Nausea; Vasopressins

Topics: Age Factors; Aged; Blood Pressure; Electrocardiography; Female; Humans; Hydrocortisone; Injections, Intravenous; Middle Aged; Nausea; Psychiatric Status Rating Scales; Schizophrenia; Vasopressins; Vomiting

Topics: Diuresis; Ethanol; Female; Humans; Muscle Contraction; Nausea; Pregnancy; Uterus; Vasopressins

Topics: Anesthetics, Local; Blood Pressure; Epinephrine; Felypressin; Hemostasis; Humans; Ischemia; Nausea; Otorhinolaryngologic Diseases; Oxytocin; Pulse; Tachycardia; Vasoconstrictor Agents; Vasopressins